The red circle shows the LAD coursing down the anterior interventricular sulcus. There is an area of dense white in the middle of the circle consistent with atherosclerosis.
The green circle here shows a small section of the RCA. The blue circle shows the LCx. They too have dense white masses consistent with coronary atherosclerosis.
Case Continued
The patient was brought back from the CT scanner with continued pain, and still appeared to be diaphoretic, short of breath, and in distress.
The emergency provider ordered another EKG at 1446 (his blood pressure at this time was about 206/103):
This EKG shows evolution of continued transmural ischemia of the inferior wall. The T wave in lead III has increased in size. There is new ST segment flattening and T wave inflation in II and aVF. The reciprocal change in aVL has become more pronounced. The T waves in V2 and V3 are starting to “deflate” suggesting posterior wall involvement.
This time, the conventional computer algorithm read:
“Normal sinus rhythm, normal ECG”.
The Queen of Hearts once again diagnoses OMI with high confidence:
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The ED provider recognized the changes in this EKG and called cardiology for a STAT consult. The cardiologist recognized that there were EKG changes, but did not take the patient for emergent catheterization because the EKG was “not meeting criteria for STEMI”.
At 1502, the first high sensitivity troponin T resulted at 18 ng/L (very slightly elevated, the URL is 16 ng/L for men in this assay).
The patient was put on a nitroglycerin drip and his pain improved with his blood pressure.
At 1554, a third EKG was ordered (At this time, his blood pressure was around 122/57):
This EKG shows changes consistent with reperfusion of the inferior wall. The T waves in leads II and aVF have deflated, and the T wave in lead III has become terminally negative. The ST depressions in I and aVL have resolved.
Smith comment: Is the ACS (rupture plaque) with occlusion that is now reperfusing? Or is it a very tight stenosis that does not allow enough flow to perfuse myocardium that has a high oxygen demand from severely elevated BP?
Transmural ischemia (as seen with the OMI findings on ECG) is not very common with demand ischemia, but is possible. The only study I'm aware of that looked at this was mine, in which 4% of Type II MI had New ST Elevation.
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Amazingly, the Queen of Hearts still diagnoses OMI, although this time with low confidence:
Case Continued by the Undergraduate:
The cardiology fellow wrote in their note: “With initial troponin just minimally elevated and resolution of chest pain as well as EKG changes with normalization of blood pressure, we have lower suspicion for an acute ischemic event. However, in light of risk factors for atherosclerotic disease and dynamic EKG changes today, we will pursue a CTCA tomorrow for further evaluation of coronaries.
It does appear more likely that his chest pain was GI in nature (possibly esophageal spasm and/or GERD) given his large meal preceding onset of chest pain, as well as CT findings consistent with large amount of ingested material in stomach.”
Smith: What???!!!
So the patient was admitted to the hospital with no plan for an angiogram.
Then at 1935 when a 2nd troponin resulted at 211 ng/L, and the patient received a diagnosis of “NSTEMI.” At 0635 the next day, a third troponin resulted at 899 ng/L. At 1041 a formal echo showed an EF of 71% and the note stated that the “basal posterior segment and and basal inferior segment are abnormal”.
The cardiology fellow wrote in their note “unclear etiology of troponin elevation at this time, but hypertensive emergency, underlying CAD with demand ischemia, or NSTEMI all remain on the differential… In light of his risk factors, concerning clinical presentation and troponin trend -- we favor coronary angiogram over CTCA at this time.”
Of course, writing “hypertensive emergency, underlying CAD with demand ischemia, or NSTEMI all remain on the differential” makes no sense. Troponin was elevated and no “STEMI” was seen on the EKG, so if it is acute MI, then “NSTEMI” is the diagnosis (however flawed), not a pathology on the differential. It is instead most likely that the patient has severe stenosis of the RCA (or possibly the LCx) and experienced such drastic hypertension that the demand could not be supplied by a severely stenosed artery, and resulted in findigs of transmural ischemia rather than subendocardial ischemia.
Smith:
After the blood pressure was controlled with nitroglycerin, the patient’s pain subsided and the EKG showed reperfusion.
Was this resolution of demand ischemia? Or was it spontaneous lysis of thrombus co-incidental with the lowering of the BP?
Probably the latter.
In any case, the appropriate intervention in this case begins with nitroglycerine, at whatever dose that it takes to lower the BP substantially.
If the pain and ECG findings do not resolve, then the cath lab is indicated.
Another EKG was taken at 1304:
This shows continued reperfusion and the development of large Q waves in lead III.
The Queen of Hearts now sees no OMI with low confidence:
